Method of treating a bacterial infection using colostrum

ABSTRACT

The method of treating a bacterial infection using colostrum includes administering an effective amount of colostrum to a subject in need thereof. The infection can be caused by G+ or G− bacteria. The colostrum administered may be selected from the group consisting of bovine colostrum, camel colostrum, and a mixture of bovine colostrum and camel colostrum. The bacterial infection may be selected from the group consisting of Staphylococcus aureus subs. aureus Rosenbach, Escherichia coli, Pseudomonas aeruginosa, and Methicillin-resistant Staphylococcus aureus. A colostrum composition can include a mixture of bone and camel colostrum and a pharmaceutically acceptable carrier.

CROSS REFERENCE TO RELATED APPLICATIONS

This application is a division of Ser. No. 16/809,882, filed Mar. 5, 2020, pending, the priority of which is claimed.

BACKGROUND 1. Field

The disclosure of the present patent application relates to a method of treating a bacterial infection by inducing an immune response.

2. Description of the Related Art

The CDC identifies antibiotic resistance as one of the most significant public health challenges of our time. In the United States alone, at least 2 million people are diagnosed with antibiotic-resistant infections annually, and at least 23,000 of these are fatal.

Strategies for developing new treatments have mostly focused on avoiding the rise of antibiotic resistance and on developing new antibiotics. However, avoiding the rise of antibiotic resistance is a failing rearguard action, given the prevalence of antibiotic-resistant bacterial strains. Further, the rate of new antibiotic development has slowed significantly. Most new classes of antibiotics were developed in the 1940s and the 1950s, with only two new classes developed since the year 2000. Antibiotics also have many undesirable side effects, ranging from nausea and diarrhea to liver and kidney damage.

Thus, a method of treating an infection solving the aforementioned problems is desired.

SUMMARY

A method of treating a bacterial infection using mixed colostrum can include administering a therapeutically effective amount of colostrum to a patient in need thereof. Administering colostrum to the patient can induce an immune response in the patient. In an embodiment, the colostrum administered may be selected from the group consisting of bovine colostrum, camel colostrum, and a mixture of bovine colostrum and camel colostrum. The infection can be bacterial. In an embodiment, the bacterial infection may be selected from the group consisting of G+ and G− bacteria: Staphylococcus aureus subs. aureus Rosenbach, Escherichia coli, Pseudomonas aeruginosa, and Methicillin-resistant Staphylococcus aureus.

An embodiment of the present subject matter is directed to a pharmaceutical composition including the mixture of bovine and camel colostrum and a pharmaceutically acceptable carrier.

An embodiment of the present subject matter is directed to a method of making a pharmaceutical composition including mixing the colostrum under sterile conditions with a pharmaceutically acceptable carrier and preservatives, buffers, or propellants to create the pharmaceutical composition; and providing the pharmaceutical composition in a form suitable for daily, weekly, or monthly administration. In an embodiment, the pharmaceutical composition may be natural and/or organic, comprising exclusively natural and/or organic ingredients

An embodiment of the present subject matter is directed to a method of treating a bacterial infection, including administering to a subject in need thereof a therapeutically effective amount of a pharmaceutical composition according to the present subject matter. The pharmaceutical composition can include a mixture of bovine and camel colostrum. In an embodiment, the pharmaceutical composition may be an organic pharmaceutical composition.

These and other features of the present disclosure will become readily apparent upon further review of the following specification and drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee.

FIG. 1 depicts a bar graph displaying IFN-γ levels in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine and camel colostrum.

FIG. 2A depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was camel colostrum.

FIG. 2B depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was bovine colostrum.

FIG. 2C depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 3 depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was bovine, camel, or a mixture of bovine colostrum and camel colostrum.

FIG. 4A depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was camel colostrum.

FIG. 4B depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was bovine colostrum.

FIG. 4C depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 5 depicts a bar graph displaying IL-10 levels in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 6A depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was camel colostrum.

FIG. 6B depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was bovine colostrum.

FIG. 6C depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to E. coli alone, and subjects exposed to both E. coli and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 7 depicts a bar graph displaying IFN-γ levels in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 8A depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was camel colostrum.

FIG. 8B depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was bovine colostrum.

FIG. 8C depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 9 depicts a bar graph displaying TNF-α levels in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 10A depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was camel colostrum.

FIG. 10B depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was bovine colostrum.

FIG. 10C depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 11 depicts a bar graph displaying IL-10 levels in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 12A depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was camel colostrum.

FIG. 12B depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was bovine colostrum.

FIG. 12C depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to P. aeruginosa alone, and subjects exposed to both P. aeruginosa and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 13 depicts a bar graph displaying IFN-γ levels in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 14A depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was camel colostrum.

FIG. 14B depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was bovine colostrum.

FIG. 14C depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 15 depicts a bar graph displaying TNF-α levels in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 16A depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was camel colostrum.

FIG. 16B depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was bovine colostrum.

FIG. 16C depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 17 depicts a bar graph displaying IL-10 levels in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 18A depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was camel colostrum.

FIG. 18B depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was bovine colostrum.

FIG. 18C depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to S. aureus alone, and subjects exposed to both S. aureus and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 19 depicts a bar graph displaying IFN-γ levels in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA, and subjects exposed to both MRSA and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 20A depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was camel colostrum.

FIG. 20B depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was bovine colostrum.

FIG. 20C depicts a bar graph displaying IFN-γ levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 21 depicts a bar graph displaying TNF-α levels in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA, and subjects exposed to both MRSA and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 22A depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was camel colostrum.

FIG. 22B depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was bovine colostrum.

FIG. 22C depicts a bar graph displaying TNF-α levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

FIG. 23 depicts a bar graph displaying IL-10 levels in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA, and subjects exposed to both MRSA and colostrum, where the colostrum was either bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum.

FIG. 24A depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was camel colostrum.

FIG. 24B depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was bovine colostrum.

FIG. 24C depicts a bar graph displaying IL-10 levels over time in control subjects, subjects exposed to colostrum alone, subjects exposed to MRSA alone, and subjects exposed to both MRSA and colostrum, where the colostrum was a mixture of camel colostrum and bovine colostrum.

Similar reference characters denote corresponding features consistently throughout the attached drawings.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

A method of treating a bacterial infection may include administering colostrum to a subject in need thereof. In an embodiment, the colostrum administered may be selected from the group consisting of bovine colostrum, camel colostrum, and a mixture of bovine colostrum and camel colostrum. In an embodiment, the infection is a bacterial infection or an infection caused by bacteria. The bacterial infection may be selected from the group consisting of G+ bacteria and G− bacteria. The bacterial infection may be selected from the group consisting of Staphylococcus aureus subs. aureus Rosenbach (S. aureus), Escherichia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa), and Methicillin-resistant Staphylococcus aureus (MRSA).

As used herein, a “subject” includes mammals, e.g., humans, dogs, cats, sheep, cows, rats, mice, and the like.

As used herein, the term “about,” when used to modify a numerical value, means within ten percent of that numerical value.

As used herein, “colostrum” is the first form of milk produced by the mammary gland of a mammal just before and/or shortly after giving birth. Colostrum contains maternal antibodies intended to protect the newborn against disease, and frequently contains significantly more protein than non-colostrum milk.

In an embodiment, the colostrum may be collected after parturition and stored at −20° C. for at least a week. In an embodiment, the colostrum may then be thawed at −4° C. for at least 8 hours, and then lyophilized. In an embodiment, the lyophilized colostrum may then be suspended in sterilized saline solution at a concentration of 28 g lyophilized colostrum per liter of sterilized saline solution, forming a colostrum composition for use as discussed herein. In an embodiment, a colostrum composition may include bovine colostrum, camel colostrum, or a mixture of bovine colostrum and camel colostrum. An embodiment of the present subject matter may include the colostrum composition including at least a mixture of one of the bovine colostrum and the camel colostrum and a pharmaceutically acceptable carrier.

In an embodiment, the administration of colostrum or a colostrum composition of the present subject matter may include daily administration. In an embodiment, the daily administration may be administered in the early morning hours. In an embodiment, administration of colostrum or a colostrum composition of the present subject matter may include injecting one ml of a solution of 28 g lyophilized colostrum per liter of sterilized saline solution every day at eight in the morning for at least a month.

In an embodiment, administration of the colostrum or colostrum composition as described herein may prevent the lethal effect of a lethal dose of an infectious bacterium. In an embodiment, the infectious bacterium may be selected from the group consisting of E. coli, P. aeruginosa, S. aureus, and MRSA.

In an embodiment, administration of the colostrum or colostrum composition of the present subject matter may stimulate the immune system. In an embodiment, the immune system stimulation may include an increase in the level of one or more cytokines in the blood. In an embodiment, the cytokines may be selected from the group consisting of Interferon-7 (IFN-γ), Tumor Necrosis Factor α (TNF-α), and Interleukin-10 (IL-10).

An embodiment of the present subject matter is directed to a pharmaceutical composition comprising the mixture of bovine and camel colostrum and a pharmaceutically acceptable carrier.

An embodiment of the present subject matter is directed to a method of making a pharmaceutical composition, including mixing an effective amount of the bovine and camel mixture colostrum with a pharmaceutically acceptable carrier. For example, the method of making a pharmaceutical composition can include mixing the colostrum under sterile conditions with a pharmaceutically acceptable carrier, preservatives, buffers, and/or propellants to create the pharmaceutical composition. In an embodiment, the pharmaceutical composition may be natural and/or organic and the pharmaceutically acceptable carrier may also be natural and/organic.

To prepare the pharmaceutical composition, at least one of the bovine colostrum and camel colostrum, as the active ingredient, is intimately admixed with a pharmaceutically acceptable carrier according to conventional pharmaceutical compounding techniques. Carriers are inert pharmaceutical excipients, including, but not limited to, binders, suspending agents, lubricants, flavorings, sweeteners, preservatives, dyes, and coatings. In preparing compositions in oral dosage form, any of the pharmaceutical carriers known in the art may be employed. For example, for liquid oral preparations, suitable carriers and additives include water, glycols, oils, alcohols, flavoring agents, preservatives, coloring agents, and the like. Further, for solid oral preparations, suitable carriers and additives include starches, sugars, diluents, granulating agents, lubricants, binders, disintegrating agents, and the like.

The present compositions can be in unit dosage forms such as tablets, pills, capsules, powders, granules, ointments, sterile parenteral solutions or suspensions, metered aerosol or liquid sprays, drops, ampules, auto-injector devices or suppositories, for oral parenteral, intranasal, sublingual or rectal administration, or for administration by inhalation or insufflation. The active compound can be mixed under sterile conditions with a pharmaceutically acceptable carrier and, if required, any needed preservatives, buffers, or propellants. The composition can be presented in a form suitable for daily, weekly, or monthly administration. The pharmaceutical compositions herein will contain, per dosage unit, e.g., tablet, capsule, powder, injection, teaspoonful, suppository and the like, an amount of the active ingredient necessary to deliver an effective dose. A therapeutically effective amount of the colostrum compositions or an amount effective to treat a disease, such as a bacterial infection, may be determined initially from the Examples described herein and adjusted for specific targeted diseases using routine methods.

The colostrum or colostrum compositions can be administered to a subject in need thereof. For example, the colostrum or colostrum compositions can be used to treat a subject suffering from a bacterial infection. The bacterial infection can be caused by E. coli, P. aeruginosa, S. aureus, MRSA, or the like.

An embodiment of the present subject matter is directed to a method of treating a bacterial infection, comprising administering to a subject in need thereof a therapeutically effective amount of the pharmaceutical composition according to the present subject matter. In an embodiment, the pharmaceutical composition may be organic.

The colostrum or pharmaceutical compositions thereof can be administered to a subject by any suitable route. For example, the colostrum or pharmaceutical compositions can be administered orally (including buccally and sublingually), nasally, rectally, intracisternally, intra-vaginally, intraperitoneally, topically, transdermally (as by powders, ointments, or drops), and/or parenterally. As used herein, “parenteral” administration refers to modes of administration other than through the gastrointestinal tract, which includes intravenous, intramuscular, intraperitoneal, intrasternal, intramammary, intraocular, retrobulbar, intrapulmonary, intrathecal, subcutaneous and intraarticular injection and infusion. Surgical implantation may also be contemplated, including, for example, embedding a composition of the disclosure in the body such as, for example, in a tissue, in the abdominal cavity, under the splenic capsule, brain, or in the cornea.

Accordingly, the route of administration can include intranasal administration, oral administration, inhalation administration, subcutaneous administration, transdermal administration, intradermal administration, intra-arterial administration with or without occlusion, intracranial administration, intraventricular administration, intravenous administration, buccal administration, intraperitoneal administration, intraocular administration, intramuscular administration, implantation administration, topical administration, intratumor administration, and/or central venous administration.

The following examples illustrate the present teachings.

Example 1 Determining the Lethal Dose and Optimum Route of Infection for Four Gram-Positive and Gram-Negative Bacteria in a Rat Model

The ethical committee of King Saud University provided prior approval before any animal studies were commenced. All animals were fed with standard laboratory rat chow (Basal diet 5755, PMI Nutrition International, Inc., Richmond, Calif., USA) according to the National Institute of Health guidelines. Rats were quarantined for six days before commencing experiments. Chemical restraint anesthesia was achieved using injectable sedation, such as a Ketamine/Xylazine mix administered subcutaneously.

The Riyadh Military Hospital Bacteriology Laboratory provided American Type Culture Collection (ATCC) Escherichia coli (E. coli) (ATTC 25922). The bacterium is Enteropathogenic E. coli (EPEC) but not Enterotoxigenic E. coli (ETEC). It does not produce verotoxin and is used for media testing and as a negative control for LT toxin production. This organism is a CLSI control strain for antimicrobial susceptibility testing. Other bacterial strains obtained from the same source include Staphylococcus aureus subsp. aureus Rosenbach (S. aureus) (ATCC 29213), Methicillin-resistant Staphylococcus aureus (MRSA) (ATCC 12498), Pseudomonas aeruginosa (P. aeruginosa) (ATCC 27853).

Bacterial propagation was performed in Trypticase Soy Broth (TSB) for seven hours at 26° C., and stock aliquots were frozen at −79° C. until used. A frozen stock sample was thawed and plated onto Trypticase Soy Blood Agar plates in preparation for a bacterial inoculum lethal dose trial using rats injected subcutaneously and intravenously. The results of this trial are compiled in Table 1 and Table 2 below.

Virus and antibody-free male Wistar rats were acquired from the Pharmacy College of King Saud University. Animals were housed up to 6 animals in a cage. Male Wistar rats (n=118) weighing 190-300 g were randomly selected to receive either intravenous (i.v.) or intraperitoneal (i.p.) injection with either E. coli or one of the other three studied bacteria (n=20-40 per group). Control rats were kept in a separate compartment. Animals were observed after bacterial injection to record the number of dead animals. The results are summarized in Table 1. At six hours after bacterial administration through either injection route, animals appeared weak and lethargic. Estimated lethal doses of each pathogenic microbe were determined as shown in Table 2. In summary, the optimized lethal doses were determined to be ˜6×10⁸/ml Colony Forming Units (CFU) for E. coli, 9×10⁸/0.5 ml CFU S. aureus, ˜9.5×10⁸/0.5 ml CFU P. aeruginosa, and 12×10⁸/1.5 ml CFU MRSA. The i.v. route of administration was preferred for all microbes.

TABLE 1 Lethal Dose in Rats Demonstration for Studied Groups Over One Week Bacterial Concentration No. Deaths strains per ml Injection Site in 1 week Escherichia 10⁸/0.5 ml i.p. (3) One-4 days coli 10⁸/1 ml (3 rats) i.p.(3) i.v.(3) Zero ATTC 25922 10⁸/2 ml (3 rats) 10⁸/3 ml (6 rats) i.p.(3) i.v.(3) One (i.v.)-7 days 10¹⁶/0.1 ml (2 rats) i.p.(3) Zero 10¹⁶/0.5 ml (1 rat) 10¹⁶/1 ml (1 rat) i.p.(2) Two-2 days 10¹⁶/1.5 ml (1 rat) 10¹⁸/1 ml (6 rats) i.p.(3) i.v.(3) Zero 10³⁶/1 ml (6 rats) i.v.(3 + 3) Three-1 day Pseudomonas 10⁸/0.5 ml (3 rats) i.p.(3) Zero aeruginosa 10⁸/1 ml (2 rats) i.p.(2) i.v.(2) One (i.v., 10⁸/2 ml) ATCC27853 10⁸/2 ml (2 rats) 1 day 10⁸/3 ml (2 rats)t i.p.(1) i.v.(1) Zero 10⁴⁰/0.1 ml (2 rats) i.p.(3) One (10⁴⁰/0.5 ml) 10⁴⁰/0.5 ml (rat) 3 days 10⁴⁰/1 ml (1 rat) i.p.(2) Zero 10⁴⁰/1.5 ml (1 rat) 10⁴⁰/0.5 ml (6 rats) i.p.(3 + 3) Three (i.v., 10⁷²) 10⁷²/0.5 ml (6 rats) i.v.(3 + 3) 3 days Staphylococcus 10⁸/0.5 ml (3 rats) i.p.(3) One-4 days aureus 10⁸/1 ml (2 rats) i.p.(2) i.v.(2) Zero ATCC12498 10⁸/2 ml (2 rats) 10⁸/3 ml (2 rats) i.p.(1) i.v.(1) Zero 10²⁰/0.1 ml (2 rats) i.p.(3) Zero 10²⁰/0.5 ml (1 rat) 10²⁰/1 ml (1 rat) i.p.(2) Zero 10²⁰/1.5 ml (1 rat) 10⁴⁰/0.5 ml (3 rats) i.v.(3 + 3) Three (i.v., 10⁶⁴/0.5 10⁶⁴/0.5 ml (3 rats) ml) 2 days Methicillin- 10⁸/0.5 ml (3 rats) i.p.(3) Zero resistant 10⁸/1 ml (2 rats) i.p.(2) i.v.(.2) Zero Staphylococcus 10⁸/2 ml (2 rats) aureus 10⁸/3 ml (2 rats) i.p.(1) i.v.(1) Zero ATCC12498 410²⁰/0.1 ml (2 rats) i.p.(3) Zero 10²⁰/0.5 ml (1 rat) 10²⁰/1 ml (1 rat) i.p.(2) Zero 10²⁰/1.5 ml (1 rat) 10⁴⁰/0.5 ml (6 rats) i.p.(3 + 3) Zero 10⁶⁴/0.5 ml (6 rats) i.v.(3 + 3) 10⁶⁰/1 ml (3 rats) i.v.(3 + 3) Zero 10⁷²/1 ml (3 rats) 10⁹⁰/1 ml (2 rats) i.p.(3) Seven-6 days 10⁹⁰/1.5 ml (1 rat) i.p.(2) 10¹²⁰/1 ml (2 rats) i.v.(2) 10¹²⁰/1.5 ml (2 rats)

TABLE 2 Recommended Lethal Dose for Studied Bacteria Concentration Injection No. Deaths Bacterial strains per ml Site in 1 Week Escherichia coli ~6 × 10⁸/ i.v. (3 rats) Three-1 day ATTC 25922   1 ml CFU/ml Pseudomonas ~9.5 × 10⁸/   i.v. (3 rats) Three-3 days aeruginosa 0.5 ml ATCC27853 CFU/ml Staphylococcus  9 × 10⁸/ i.v. (3 rats) Three-2 days aureus 0.5 ml ATCC12498 CFU/ml Methicillin- 12 × 10⁸/ i.v. (3 rats) Three-6 days resistant 1.5 ml Staphylococcus CFU/ml aureus ATCC12498

Example 2 Determining Effect of Camel Colostrum, Bovine Colostrum, and a Mixture of Camel Colostrum and Bovine Colostrum on Survival of Rats Infected with Gram-Positive and Gram-Negative Bacteria

Three types of colostrum were used from different sources. Camel colostrum was sourced from 10 healthy individual camels (Camelus dromedarius) that were chosen randomly (average age, six years) from the Conservation and Genetic Improvement Center in Al-karj, Saudi Arabia. Samples were obtained manually from all camels' udders and were collected immediately after parturition.

Bovine colostrum samples were sourced from 10 healthy Holstein cows (average age, 3.8 years) provided by the Almarai Company. The Immunology Lab, King Khaled Hospital, Medicine College, King Saud University Hospital, collected the samples and confirmed that the source cows were in good health and had no clinical evidence of mastitis or tuberculosis, delivered healthy full-term infants, and had not consumed medications within one week before collection.

The colostrum samples were collected using the following protocol: 20 samples collected at the first-day parturition after thorough hand washing and cleansing of the breast and nipple with soap and tap water. Milk samples were expressed manually into sterile Erlenmeyer flasks, pooled, dispensed into sterile test tubes and stored on at −20° C.

The study included a control group with no graft contamination and no antibiotic prophylaxis (Group 1), a bacterial treatment group (Group 2), a colostrum treatment group (Group 3), and a bacterial treatment and colostrum treatment group (Group 4). (See Table 3) Group 3 included three different sub-groups, designated camel colostrum, bovine colostrum, and mix colostrum. One ml of prepared colostrum solution (28 g lyophilized colostrum/liter sterilized saline solution (w/v)) was administered by intraperitoneal injection every day early in the morning for 30 days.

The rats of Group 2 and Group 4 were then anesthetized with chloroform or ether and injected intravenously with the recommended lethal dose of one of the studied bacteria in the tail vein. Survival rates in each group were observed for two weeks after injection.

TABLE 3 The Study Groups Group 1 Control group: Sterilized saline was administered every day at eight AM for 30 days Group 2 Bacterial groups: four bacterial sub-groups were designated, one for each bacterium: Escherichia coli ATTC 25922 Pseudomonas aeruginousa ATCC27853 Staphylococcus aureus ATCC12498 Methicillin-resistant Staphylococcus aureus ATCC12498 The lethal dose of each bacterium established in Table 1 was administered intravenously once in the tail vein of each rat using a 14-gauge needle at eight AM on the starting day. Group 3 Colostrum groups: Three colostrum sub-groups were designated: Camel Colostrum Bovine Colostrum Mix Colostrum One ml of prepared colostrum solution (28 g lyophilized colostrum/liter sterilized saline solution (w/v)) was injected i.p. daily at eight AM for 30 days. Group 4 Bacterial and Colostrum groups: Sub-groups were designated for all possible combinations of Group 2 and Group 3.

At zero time up to one month and after inoculation with the four studied bacteria and induction by colostrum as in Table 4 and Table 5, animals appeared weak and lethargic with the microbial treatments. In controls without bacterial treatment, camel colostrum, bovine colostrum, and mix (a mixture of both camel and bovine colostrum) produced a similar survival rate without evidence of concentration of disease (See Table 4). Compared with the control treatment, bacterial treatment with colostrum improved mortality rates associated with the bacterial variable and route of treatment. These animals lived through one month of observation. The death of animals started from the second day until the 22^(nd) day, with most deaths occurring in the administrated pathogenic bacteria only group (Group 2). As shown in Table 4, the fastest and the best-protected treatment was lethal S. aureus with 50-100% mortality.

Moreover, 100% of rats injected with S. aureus and vaccinated i.p. by one of the three types of colostrum survived. Camel colostrum had a tremendous protective effect from lethal MRSA, converting 100% mortality to 100% survival. Camel and bovine colostrum enhanced survival against lethal P. aeruginosa from 0% to 33% survival in the former and from 50% to 66% survival in the latter (see Table 4). Lethal E. coli caused 84% mortality, and camel colostrum enhanced survival of up to 83%. On the other hand, mixed colostrum also enhanced survival, up to 50%.

TABLE 4 Morbidity and Mortality (Survival %) in Lethal Dose Induction for Four Pathogenic Bacteria using Three Colostrum Groups as Anti-Microbial Agents Colostrum Bacteria Healthy Bacteria & Colostrum Healthy Dose Rats per Healthy Healthy Rats or Dead(Day) Rats or Dead(Day) Rats (~CFU/ml) Group Rats Camel Bovine Mix Camel Bovine Mix Camel Bovine Mix E. coli: 6 6 6 6 6 6 2(3) 6 1(2) 1(2)  3(22) 6 × 10⁸/ml 2(7) 2(9)   1(13) 3(16) % Survival 100 100 100 100 100 100  16 100 83 0 50 P. aeruginosa: 6 6 6 6 6 2(2) 1(2) 6 2(5) 2(20) 6 9.5 × 10⁸/0.5 ml 3(3) 1(8) 1(9) 1(7)  1(15)  1(11) % Survival 100 100 100 100 100 0 50 100 33 66 100 S. aureus 6 6 6 6 6 1(3) 2(4) 1(3) 6 6 6 9 × 10⁸/0.5 ml 1(5) 2(7) 1(4)  1(17)  1(10)  1(12)  1(11) % Survival 100 100 100 100 100 50   0 50 100 100 100 MRSA: 6 6 6 6 6 2(2)  6 6 6 6 6 12 × 10⁸/1.5 ml 1(4) 1(8)  1(12)  1(16) % Survival 100 100 100 100 100 0 100  100 100 100 100

Example 3 Determining Effect of Camel Colostrum, Bovine Colostrum, and a Mixture of Camel Colostrum and Bovine Colostrum on Percentage Change in Weight of Rats Infected with Gram-Positive and Gram-Negative Bacteria

The effect of the treatment on the percentage change of the weight of rats (grams) for each studied pathogenic bacterium was determined using three types of colostrum; Camel, Bovine, and Mix. The results of this experiment are illustrated in Table 5 and Table 6. The range of percent change in the weight of healthy rats was revealed in minimum and maximum (Min 10%-Max 29%) through one month of observation. Camel colostrum and Mix colostrum induced a remarkable 6%-59% increase in the weight of rats. Bacterial injections dramatically decreased the percent weight change in rats from −12% to 12%. The most notable max increase values in percent change of weight of rats after colostrum treatment were observed when comparing the weight of rats infected with MRSA alone with the weight of the rats treated with mix colostrum. Mix colostrum induced 43% change in the weight of rats compared to −21% weight change in rats injected with a lethal dose of MRSA alone.

TABLE 5 Treatment Effects on Average % Change in Weight (g) of Rats (Healthy & Bacteria Treatment Groups) Group Healthy Bacteria Day 1 10 20 30 Avg % 1 10 20 30 Avg % Camel Colostrum E. coli 226 256 276 292 29% 210 205 209 214 1.9 P. aeruginosa 236 215 250 287 21% 228 232 230 245 7.4 S. aureus 227 205 228 250 10% 230 239 243 235 2.1 MRSA 235 225 247 290 23% 207 210 222 205 −0.9 Bovine Colostrum E. coli 226 256 276 292 29% 215 224 230 235 9.3 P. aeruginosa 236 215 250 287 21% 234 230 227 220 −5.9 S. aureus 251 205 228 250 10% 215 224 230 235 9.3 MRSA 235 225 247 290 23% 234 230 227 220 −5.9 Mix Colostrum E. coli 226 256 276 292 29% 242 250 267 259 7 P. aeruginosa 236 215 250 287 21% 247 255 247 279 12 S. aureus 251 205 228 250 10% 273 249 231 213 −21 MRSA 235 225 247 290 23% 252 270 263 267 5.9

TABLE 6 Treatment Effects on Average % Change in Weight (g) of Rats (Bacteria & Colostrum and Colostrum Treatment Groups) Group Bacteria & Colostrum Colostrum Day 1 10 20 30 Avg % 1 10 20 30 Avg % Camel Colostrum E. coli 227 235 245 240 5.7%  213 246 278 286 34 P. aeruginosa 260 252 254 259 −0.3%  227 239 345 354 55 S. aureus 234 239 244 260 11% 243 275 288 295 21 MRSA 250 253 255 259 3.6%  252 258 261 269 6 Bovine Colostrum E. coli 236 264 285 298 26% 230 236 254 270 17 P. aeruginosa 241 265 273 295 37% 242 265 277 293 21 S. aureus 236 264 285 298 26% 230 236 254 270 17 MRSA 241 265 273 295 22.4 218 244 279 298 36 Mix Colostrum E. coli 270 284 312 326 20% 205 240 276 288 40 P. aeruginosa 234 255 288 310 32% 272 281 301 321 18 S. aureus 230 252 284 329 43% 209 225 246 280 33 MRSA 202 235 272 280 38% 193 225 286 307 59

Example 4

Effect of Infection and/or Colostrum on Expression of Three Cytokines in Rats

For circulating blood analysis, animals were anesthetized with an ether mask. Circulating levels of IFN-γ, IL-10, and TNF-α were measured in serum samples of all rats obtained from the eye vein. Blood samples were collected in heparinized syringes to asses cytokine level assessed of IFN-γ, IL10, and TNF-α. Serum concentrations of each cytokine were monitored at 0 days post-treatment, 24 hours post-treatment, 7-25 days post-treatment (midpoint or Mid), and 30 days post-treatment (Last or Final) by ELISA. Briefly, blood samples (2 ml) were centrifuged for 10 minutes at 3500 rpm, at 4° C., and the serum samples were kept at −20° C. in a freezer until examined. Commercial reagents used to identify individual cytokines included Quantikine®ELISA, Rat TNF-α Immunoassay, Catalog Number RTA00, Quantikine®ELISA, Rat IL-10 Immunoassay, Quantikine®ELISA, and Rat IFN-γ Immunoassay. These kits were used according to the manufacturer's recommendations (USA & Canada R&D Systems, Inc. Minneapolis). The limits of sensitivity of the assay were determined to be five pg/ml for TNF-α and ten pg per ml for IFN-γ and IL-10, respectively. The intra- and inter-assay coefficients of deviation were less than 5% and 10%, respectively.

Quantitative data were statistically represented in terms of minimum, maximum, and median. A comparison between different groups in the present study was done using the Kruskal-Wallis test to compare between more than two nonparametric groups.

Correlation between various variables was determined using Spearman rank correlation coefficient (R) with graph representations using linear regression.

A probability value (p-value) less than or equal to 0.05 was considered significant. All statistical analyses were performed using statistical software SPSS (Statistical Package for Social Science) statistical program version 16.0. Graphs were created using SPSS statistical program version 16.0 with Microsoft Excel program version 2010.

Initial results for IFN-γ expression as a measure of the immune response in the presence of colostrum, E. coli, or E. coli and colostrum are presented in Table 7 and FIG. 1 .

TABLE 7 E. Coli and IFN-y Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Camel Bovine Mix P Type Colostrum Colostrum Colostrum value^(A) Healthy 2.20 2.20 2.20 1.000 Control  (0.00-43.91)  (0.00-43.91)  (0.00-43.91) Colostrum 0.00 0.09 17.82 0.055 (0.00-0.03)   (0.00-209.50)   (0.00-125.00) Bacteria 0.02 0.06 0.11 0.219 (0.00-0.07)  (0.01-74.24)   (0.00-125.00) Colostrum 0.01 0.06 0.12 0.098 & (0.00-0.03)   (0.00-117.10)  (0.00-93.75) Bacteria P value^(B) 0.018 0.808 0.901 ^(A)=Comparison between different treatments within a single colostrum type using a nonparametric test (Kruskal-Wallis Test). ^(B)=Comparison between different colostrum types in each treatment using a nonparametric test (Kruskal-Wallis Test).

Data from the full month-long experiment are presented in Table 8 and FIGS. 2A-2C. In the model of E. coli bacterial infection treated with either bovine colostrum or with the mixed colostrum, IFN-γ elevated up to 0.12 pg/ml in the mixed colostrum treatment group but was 0.06 pg/ml in the bovine colostrum treatment group. At the end of the trial (Last) IFN-γ exhibited a steady level of the immune response in the mixed colostrum treatment group (93.750 pg/ml) as well as the bacterial infection and mixed colostrum treatment group. (See Table 8). This experiment confirms the synergistic effect of mixed colostrum, as it triggers a more significant immune response than bovine colostrum or camel colostrum alone.

TABLE 8 E. coli and IFN-γ Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median (Min-Max) Treatment Group Time Camel Bovine Mix Healthy  0 h 1.496 1.496 1.496 (0.220-2.770) (0.220-2.770) (0.220-2.770) 24 h 3.587 3.587 3.587 (1.630-5.550) (1.630-5.550) (1.630-5.550) M 42.175 42.175 42.175 (40.440-43.910) (40.440-43.910) (40.440-43.910) Last 0.005 0.005 0.005 (0.000-0.010) (0.000-0.010) (0.000-0.010) P value 0.104 0.104 0.104 Colostrum  0 h 0.019 1.055 3.129 (0.010-0.030) (0.120-1.990) (0.000-6.260) 24 h 0.002 0.058 1.667 (0.000-0.000) (0.060-0.060) (0.000-3.330) M 0.002 128.800 30.327 (0.000-0.000)  (48.10-209.50) (29.390-31.260) Last 0.005 0.001 93.750 (0.000-0.010) (0.000-0.000)  (62.50-125.00) P value 0.160 0.078 0.106 Bacteria  0 h 0.025 1.019 0.003 (0.010-0.040) (0.050-1.990) (0.000-0.000) 24 h 0.003 0.051 0.003 (0.000-0.010) (0.040-0.070) (0.000-0.000) M 0.016 37.183 19.633 (0.000-0.030)  (0.130-74.240)  (0.200-39.060) Last 0.049 0.013 125.00 (0.020-0.070) (0.010-0.020) (125.00-125.00) P value 0.280 0.139 0.103 Colostrum  0 h 0.018 0.048 0.061 & (0.010-0.030) (0.020-0.070) (0.000-0.120) Bacteria 24 h 0.001 0.067 0.008 (0.000-0.000) (0.040-0.090) (0.010-0.010) M 0.016 77.905 20.840 (0.000-0.030)  (38.71-117.10) (20.840-20.840) Last 0.000 0.012 93.750 (0.000-0.000) (0.000-0.020) (93.750-93.750) P value 0.165 0.104 0.362

In the model of E. coli bacterial infection, both camel colostrum and mixed colostrum stimulated TNF-α. The highest enhancement was for camel colostrum in all treatments (0.56 pg/ml, 0.57 pg/ml, and 0.60 pg/ml for colostrum alone, bacteria alone, and colostrum with bacteria, respectively). These results are summarized in Table 9 and FIG. 3 . Data from the full month-long experiment are presented in FIGS. 4A-4C.

TABLE 9 E. coli and TNF-α Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum P Type Camel Bovine Mix value^(A) Healthy 0.00 0.00 0.00 1.000 (0.00-0.60) (0.00-0.60) (0.00-0.60) Colostrum 0.56 0.00 0.03 0.261 (0.00-0.94)   (0.00-194.80) (0.00-0.62) Bacteria 0.57 0.00 0.18 0.033 (0.00-1.13) (0.00-0.22) (0.00-0.96) Colostrum & 0.60 0.00 0.23 0.002 Bacteria (0.25-1.00) (0.00-0.00) (0.00-0.76) P value^(B) 0.101 0.331 0.373 ^(A)=Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)=Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

In the model of E. coli bacterial infection, mixed colostrum alone triggered the IL-10 immune response more than the other treatments (83.30 pg/ml). The most enormous increase was observed in the presence of mixed colostrum and E. coli bacteria (1000.0 pg/ml at the Last point). (See Table 10 and FIG. 5 )

TABLE 10 E. coli and IL-10 Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum P Type Camel Bovine Mix value^(A) Healthy 0.00 0.00 0.00 1.000 (0.00-36.76) (0.00-36.76) (0.00-36.76)   Colostrum 0.00 0.14 83.30 0.115 (0.00-16.30) (0.00-38.65) (0.00-1000.00) Bacteria 0.00 0.02 31.62 0.159 (0.00-0.64)  (0.00-0.26)  (0.00-1000.00) Colostrum & 0.00 0.01 0.01 0.290 Bacteria (0.00-0.14)  (0.00-0.29)  (0.00-1000.00) P value^(B) 0.750 0.353 0.632 ^(A)=Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)=Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

Data from the full month-long experiment are presented in Table 11 and FIGS. 6A-6C. IL-10 started to increase after 24 hours in the bacterial infection with 80.308 pg/ml. Moreover, colostrum continued to induce IL-10 from 7 days-25 days up to 166.60 pg/ml.

TABLE 11 E. coli and IL-10 Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median (Min-Max)) Treatment Group Time Camel Bovine Mix Healthy 0 h 0.016 0.016 0.016 (0.000-0.030) (0.000-0.030) (0.000-0.030) 24 h 18.378 18.378 18.378  (0.000-36.760)  (0.000-36.760)  (0.000-36.760) M 0.018 0.018 0.018 (0.000-0.030) (0.000-0.030) (0.000-0.030) Last 0.004 0.004 0.004 (0.000-0.010) (0.000-0.010) (0.000-0.010) P value 0.935 0.935 0.935 Colostrum 0 h 0.000 19.621 0.001 (0.000-0.000)  (0.590-38.650) (0.000-0.000) 24 h 0.000 0.810 0.002 (0.000-0.000) (0.150-1.470) (0.000-0.000) M 8.152 0.077 166.63  (0.000-16.300) (0.020-0.130) (166.60-166.66) Last 0.005 0.001 750.0 (0.000-0.000) (0.000-0.000)  (500.0-1000.0) P value 0.105 0.104 0.091 Bacteria 0 h 0.000 0.156 0.010 (0.000-0.000) (0.050-0.260) (0.000-0.020) 24 h 0.318 0.017 80.308 (0.000-0.640) (0.010-0.020) (63.220-97.400) M 0.009 0.044 0.001 (0.000-0.020) (0.020-0.070) (0.000-0.000) Last 0.056 0.002 750.0 (0.060-0.060) (0.000-0.000)  (500.0-1000.0) P value 0.467 0.139 0.080 Colostrum 0 h 0.000 0.162 0.005 & (0.000-0.000) (0.030-0.290) (0.000-0.010) Bacteria 24 h 0.000 0.010 0.013 (0.000-0.000) (0.010-0.010) (0.010-0.010) M 0.006 0.010 0.001 (0.000-0.010) (0.010-0.010) (0.000-0.000) Last 0.089 0.006 1000.0 (0.040-0.140) (0.000-0.010) (1000.0-1000.0) P value 0.116 0.276 0.284

In the model of P. aeruginosa infection, the mixed colostrum induced IFN-γ expression of 17.82 pg/ml. Further, the mixed colostrum combined with bacterial infection resulted in an IFN-γ expression of 32.22 pg/ml. These results are presented in Table 12 and FIG. 7 . Data from the full month-long experiment are presented in FIGS. 8A-8C.

TABLE 12 P. aeruginosa and IFN-γ Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum P Type Camel Bovine Mix value^(A) Healthy 2.20 2.20 2.20 1.000  (0.00-43.91)  (0.00-43.91)  (0.00-43.91) Colostrum 0.00 0.09 17.82 0.055 (0.00-0.03)   (0.00-209.50)   (0.00-125.00) Bacteria 0.01 0.07 0.50 0.284  (0.00-74.40)   (0.02-105.79)  (0.01-62.50) Colostrum 0.00 0.06 32.22 0.002 & (0.00-0.00) (0.03-0.49)   (0.00-457.20) Bacteria P value^(B) 0.007 0.712 0.578 ^(A)=Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)=Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

In the model of P. aeruginosa infection, the most considerable enhancement of TNF-α expression was detected in the group administered camel colostrum, which demonstrated 0.56 pg/ml, 1.54 pg/ml and 1.00 pg/ml for colostrum treatment alone, bacterial treatment alone, and colostrum and bacterial treatment, respectively. These results are presented in Table 13 and FIG. 9 .

TABLE 13 P. aeruginosa and TNF-α Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum P Type Camel Bovine Mix value^(A) Healthy 0.00 0.00 0.00 1.000 (0.00-0.60) (0.00-0.60) (0.00-0.60) Colostrum 0.56 0.00 0.03 0.261 (0.00-0.94)   (0.00-194.80) (0.00-0.62) Bacteria 1.54 0.00 0.00 0.004 (0.54-1.91) (0.00-0.00) (0.00-1.09) Colostrum& 1.00 0.00 0.55 0.006 Bacteria  (0.00-12.50) (0.00-0.00) (0.00-4.58) P value^(B)  0.025  0.185  0.663 ^(A)=Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)=Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

Data from the month-long experiment are presented in Table 14 and FIGS. 10A-10C. P. aeruginosa administration increased TNF-α expression after 24 hours to 1.171 pg/ml. In comparison, an expression level of 0.828 pg/ml was detected for camel colostrum administration. The most efficient change in TNF-α expression was observed for the administration of both camel colostrum and P. aeruginosa (8.931 pg/ml 24 hours after administration of the bacterium).

TABLE 14 P. aeruginosa and TNF-α Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.300 0.300 0.300 (0.000-0.600) (0.000-0.600) (0.000-0.600) 24 h 0.220 0.220 0.220 (0.000-0.440) (0.000-0.440) (0.000-0.440) M 0.269 0.269 0.269 (0.000-0.540) (0.000-0.540) (0.000-0.540) Last 0.000 0.000 0.000 (0.000-0.000) (0.000-0.000) (0.000-0.000) P value 0.675 0.675 0.675 Colostrum 0 h 0.558 0.000 0.000 (0.540-0.580) (0.000-0.000) (0.000-0.000) 24 h 0.828 0.000 0.000 (0.720-0.940) (0.000-0.000) (0.000-0.000) M 0.430 104.749 0.177 (0.170-0.690)  (14.70-194.80) (0.050-0.300) Last 0.000 0.000 0.490 (0.000-0.000) (0.000-0.000) (0.360-0.620) P value 0.108 0.077 0.078 Bacteria 0 h 1.594 0.000 0.000 (1.280-1.910) (0.000-0.000) (0.000-0.000) 24 h 1.171 0.000 0.000 (0.540-1.800) (0.000-0.000) (0.000-0.000) M — 0.000 0.185 (0.000-0.000) (0.000-0.360) Last — 0.000 0.550 (0.000-0.000) (0.010-1.090) P value 0.439 1.000 0.100 Colostrum 0 h 0.769 0.000 0.000 & (0.540-1.000) (0.000-0.000) (0.000-0.000) Bacteria 24 h 8.931 0.000 0.000  (5.360-12.500) (0.000-0.000) (0.000-0.000) M 0.861 0.000 2.568 (0.360-1.360) (0.000-0.000) (0.550-4.580) Last 0.000 0.000 0.695 (0.000-0.000) (0.000-0.000) (0.560-0.830) P value 0.185 1.000 0.183

In the model of P. aeruginosa infection, the administration of the mixture of colostrum alone caused the greatest change in IL-10 levels (83.30 pg/ml), as shown in Table 15 and FIG. 11 . Data from the month-long experiment are presented in Table 16 and FIGS. 12A-12C.

TABLE 15 P. aeruginosa and IL-10 Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum P Type Camel Bovine Mix value^(A) Healthy 0.00 0.00 0.00 1.000  (0.00-36.76)  (0.00-36.76) (0.00-36.76)   Colostrum 0.00 0.14 83.30 0.115  (0.00-16.30)  (0.00-38.65)   (0.00-1000.00) Bacteria 0.00 0.01 0.07 0.019 (0.00-0.01) (0.01-0.03) (0.00-500.00)  Colostrum & 0.00 0.08 1.31 0.388 Bacteria  (0.00-72.69) (0.00-1.67) (0.00-500.00)  P value^(B) 0.749 0.321 0.286 ^(A)=Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)=Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

TABLE 16 P. aeruginosa and IL-10 Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.016 0.016 0.016 (0.000-0.030) (0.000-0.030) (0.000-0.030) 24 h 18.378 18.378 18.378  (0.000-36.760)  (0.000-36.760)  (0.000-36.760) M 0.018 0.018 0.018 (0.000-0.030) (0.000-0.030) (0.000-0.030) Last 0.004 0.004 0.004 (0.000-0.010) (0.000-0.008) (0.000-0.010) P value 0.935 0.935 0.935 Colostrum 0 h 0.000 19.621 0.001 (0.000-0.000)  (0.590-38.650) (0.000-0.000) 24 h 0.000 0.810 0.002 (0.000-0.000) (0.150-1.470) (0.000-0.000) M 8.152 0.077 166.63  (0.000-16.300) (0.020-0.130) (166.60-166.66) Last 0.005 0.001 750.00 (0.000-0.000) (0.001-0.001)  (500.0-1000.0) P value 0.105 0.104 0.091 Bacteria 0 h 0.001 0.020 0.029 (0.001-0.001) (0.010-0.030) (0.020-0.040) 24 h 0.004 0.007 8.914 (0.000-0.008) (0.010-0.010)  (0.070-17.760) M — 0.008 83.301 (0.010-0.010)   (0.000-166.600) Last — 0.009 500.00 (0.010-0.010) (500.00-500.00) P value 1.000 0.701 0.375 Colostrum 0 h 0.000 0.008 0.043 & (0.000-0.000) (0.000-0.020) (0.040-0.050) Bacteria 24 h 36.414 1.173 3.653  (0.140-72.690) (0.670-1.670) (2.570-4.740) M 3.601 0.030 0.002 (0.000-7.200) (0.030-0.030) (0.001-0.002) Last 0.002 0.128 500.00 (0.000-0.000) (0.130-0.130) (500.00-500.00) P value 0.297 0.194 0.080

In the model of S. aureus subsp. aureus Rosenbach infection, IFN-γ levels increased to 78.10 pg/ml when the mixed colostrum and bacteria were administered, as compared to 17.82 pg/ml when the mixed colostrum alone was administered (see Table 17 and FIG. 13 ).

TABLE 17 S. aureus and IFN-γ Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Type: Camel Bovine Mix P value^(A) Healthy 2.20(0.00-43.91) 2.20(0.00-43.91) 2.20(0.00-43.91) 1.000 Colostrum 0.00(0.00-0.03)   0.09(0.00-209.50) 17.82(0.00-125.00) 0.055 Bacteria 0.01(0.00-64.78) 0.44(0.04-75.23) 0.50(0.01-62.50) 0.076 Colostrum & 0.02(0.00-2.91)  23.76(0.01-94.87)   78.10(0.03-6541.00) 0.008 Bacteria P value^(B) 0.026 0.436 0.362 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

In the month-long experiment, administration of the mixture of colostrum and S. aureus resulted in an increased level of IFN-γ of 3333.0 pg/ml by the final time-point. In comparison, at days 7-25 (M), the median IFN-γ level of rats administered mixed colostrum and S. aureus was 278.15 pg/ml. At the 24 hour time-point this level was only 15.647 pg/ml. These results are presented in Table 18 and FIGS. 14A-14C.

TABLE 18 S. aureus and IFN-γ Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 1.496(0.220-2.770) 1.496(0.220-2.770) 1.496(0.220-2.770) 24 h 3.587(1.630-5.550) 3.587(1.630-5.550) 3.587(1.630-5.550) M  42.175(40.440-43.910)  42.175(40.440-43.910)  42.175(40.440-43.910) Last 0.005(0.000-0.010) 0.005(0.000-0.010) 0.005(0.000-0.010) P value 0.104 0.104 0.104 Colostrum 0 h 0.019(0.008-0.030) 1.055(0.120-1.990) 3.129(0.000-6.260) 24 h 0.002(0.000-0.004) 0.058(0.060-0.060) 1.667(0.000-3.330) M 0.002(0.001-0.002) 128.800(48.10-209.50)   30.327(29.390-31.260) Last 0.005(0.003-0.006) 0.001(0.001-0.001) 93.750(62.50-125.00) P value 0.160 0.078 0.106 Bacteria 0 h 32.400(0.020-64.780)  6.787(0.090-13.480) 0.194(0.110-0.280) 24 h 0.066(0.001-0.130) 0.356(0.050-0.670) 2.022(0.710-3.330) M 0.005(0.003-0.007) 2.241(0.210-4.270) 10.450(0.070-20.830) Last 0.002(0.000-0.002) 37.639(0.040-75.230) 31.256(0.010-62.500) P value 0.426 0.919 0.881 Colostrum & 0 h 1.558(0.210-2.910) 47.440(0.010-94.870) 0.140(0.030-0.250) Bacteria 24 h 0.010(0.000-0.010) 0.355(0.360-0.360) 15.647(0.090-31.200) M 0.008(0.000-0.010)  18.174(12.590-23.760)  278.15(173.90-382.40) Last 0.033(0.020-0.050)  46.956(37.680-56.230) 3333.00(125.0-6541.0)  P value 0.106 0.587 0.139

In the model of S. aureus subsp. aureus Rosenbach infection, the most excellent enhancement in TNF-α levels was observed after administration of camel colostrum, which had 0.56 pg./m., 1.21 pg./m and 0.50 pg./m for Colostrum, Bacteria, and Colostrum with Bacteria respectively (See Table 19 and FIG. 15 ). Data from the month-long experiment are presented in Table 20 and FIGS. 16A-16C.

TABLE 19 S. aureus and TNF-α Immune Response in the Presence of Colostrum (expressed as median pg/ml (Min-Max)) Colostrum Type: P Camel Bovine Mix value^(A) Healthy 0.00(0.00-0.60) 0.00(0.00-0.60)  0.00(0.00-0.60)  1.000 Colostrum 0.56(0.00-0.94) 0.00(0.00-194.80) 0.03(0.00-0.62)  0.261 Bacteria 1.21(0.00-9.85) 0.00(0.00-0.00)  0.00(0.00-1.09)  0.002 Colostrum 0.50(0.00-6.55) 0.00(0.00-0.00)  0.12(0.00-116.44) 0.014 & Bacteria P value^(B) 0.043 0.118 0.931 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

TABLE 20 S. aureus and TNF-α Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.300(0.000-0.600) 0.300(0.000-0.600) 0.300(0.000-0.600) 24 h 0.220(0.000-0.440) 0.220(0.000-0.440) 0.220(0.000-0.440) M 0.269(0.000-0.540) 0.269(0.000-0.540) 0.269(0.000-0.540) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.000(0.000-0.000) P value 0.675 0.675 0.675 Colostrum 0 h 0.558(0.540-0.580) 0.000(0.000-0.000) 0.000(0.000-0.000) 24 h 0.828(0.720-0.940) 0.000(0.000-0.000) 0.000(0.000-0.000) M 0.430(0.170-0.690) 104.749(14.70-194.80)  0.177(0.050-0.300) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.490(0.360-0.620) P value 0.108 0.077 0.078 Bacteria 0 h 5.930(2.010-9.850) 0.000(0.000-0.000) 0.000(0.000-0.000) 24 h 0.962(0.720-1.210) 0.000(0.000-0.000) 0.000(0.000-0.000) M 0.900(0.580-1.220) 0.000(0.000-0.000) 0.185(0.000-0.360) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.550(0.010-1.090) P value 0.185 1.000 0.100 Colostrum & 0 h 6.184(5.820-6.550) 0.000(0.000-0.000) 0.000(0.000-0.000) Bacteria 24 h 0.600(0.580-0.620) 0.000(0.000-0.000) 0.000(0.000-0.000) M 0.352(0.280-0.430) 0.000(0.000-0.000)  58.336(0.230-116.440) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.589(0.560-0.620) P value 0.080 1.000 0.109

In the model of S. aureus subsp. aureus Rosenbach infection, treatment with mixed colostrum alone and treatment with mixed colostrum and bacteria led to the highest increase in IL-10 levels (See Table 21 and FIG. 17 ).

TABLE 21 S. aureus and IL-10 Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Type: Camel Bovine Mix P value^(A) Healthy  0.00(0.00-36.76)  0.00(0.00-36.76) 0.00(0.00-36.76) 1.000 Colostrum  0.00(0.00-16.30)  0.14(0.00-38.65)  83.30(0.00-1000.00) 0.115 Bacteria 0.00(0.00-0.98)  0.04(0.00-23.78)  0.07(0.00-500.00) 0.023 Colostrum & Bacteria 0.00(0.00-0.07) 0.03(0.00-0.39)  83.38(0.01-1000.00) 0.021 P value^(B) 0.677 0.428 0.153 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

In the month-long experiment, treatment with mixed colostrum and treatment with either mixed colostrum alone or with mixed colostrum and bacteria resulted in a similar increase in IL-10 levels (166.63 and 166.60 respectively at 7-25 days and 750.00 pg/ml at the end of the month). These results are presented in Table 22 and FIGS. 18A-18C.

TABLE 22 S. aureus and IL-10 Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.016(0.000-0.030) 0.016(0.000-0.030) 0.016(0.000-0.030) 24 h 18.378(0.000-36.760) 18.378(0.000-36.760) 18.378(0.000-36.760) M 0.018(0.000-0.030) 0.018(0.000-0.030) 0.018(0.000-0.030) Last 0.004(0.000-0.010) 0.004(0.000-0.010) 0.004(0.000-0.010) P value 0.935 0.935 0.935 Colostrum 0 h 0.000(0.000-0.000) 19.621(0.590-38.650) 0.001(0.001-0.001) 24 h 0.000(0.000-0.000) 0.810(0.150-1.470) 0.002(0.001-0.002) M  8.152(0.000-16.300) 0.077(0.020-0.130)  166.63(166.60-166.66) Last 0.005(0.005-0.005) 0.001(0.000-0.001) 750.00(500.0-1000.0) P value 0.105 0.104 0.091 Bacteria 0 h 0.491(0.000-0.980) 0.089(0.010-0.170) 0.029(0.020-0.040) 24 h 0.000(0.000-0.000) 0.040(0.020-0.060)  8.914(0.070-17.760) M 0.000(0.000-0.000) 11.890(0.000-23.780)  83.301(0.000-166.600) Last 0.009(0.010-0.010) 0.103(0.010-0.200)  500.00(500.00-500.00) P value 0.166 0.983 0.375 Colostrum & 0 h 0.001(0.000-0.000) 0.216(0.040-0.390) 0.010(0.010-0.010) Bacteria 24 h 0.000(0.000-0.000) 0.012(0.000-0.020) 0.085(0.010-0.160) M 0.001(0.000-0.000) 0.045(0.020-0.070)  166.60(166.60-166.60) Last 0.053(0.040-0.070) 0.000(0.000-0.000) 750.00(500.0-1000.0) P value 0.143 0.276 0.100

In the model of MRSA infection, the administration of a lethal dose of MRSA also raised IFN-7 levels to 78.13 pg/ml when treated with mixed colostrum and bacteria. These results are similar to the IFN-7 levels reported above for rats administered a combination of mixed colostrum and S. aureus of 78.10 pg/ml. This result compares favorably to the IFN-γ levels reported for rats administered Bovine Colostrum and S. aureus of 23.76 pg/ml. Thus, these results confirm the improved immune response to treatment with mixed colostrum. The MRSA experimental results are summarized in Table 23 and FIG. 19 . The month-long MRSA experimental results are summarized in Table 24 and FIGS. 20A-20C.

TABLE 23 MRSA and IFN-γ Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Type: Camel Bovine Mix P value^(A) Healthy  2.20(0.00-43.91) 2.20(0.00-43.91)  2.20(0.00-43.91) 1.000 Colostrum 0.00(0.00-0.03)  0.09(0.00-209.50)  17.82(0.00-125.00) 0.055 Bacteria 0.01(0.00-0.07) 0.57(0.01-25.05) 0.01(0.00-0.07) 0.024 Colostrum & Bacteria 0.00(0.00-0.87) 0.08(0.00-38.71)  78.13(0.01-300.06) 0.004 P value^(B) 0.009 0.646 0.057 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

TABLE 24 MRSA and IFN-γ Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 1.496(0.220-2.770) 1.496(0.220-2.770) 1.496(0.220-2.770) 24 h 3.587(1.630-5.550) 3.587(1.630-5.550) 3.587(1.630-5.550) M  42.175(40.440-43.910)  42.175(40.440-43.910)  42.175(40.440-43.910) Last 0.005(0.000-0.010) 0.005(0.000-0.010) 0.005(0.000-0.010) P value 0.104 0.104 0.104 Colostrum 0 h 0.019(0.010-0.030) 1.055(0.120-1.990) 3.129(0.000-6.260) 24 h 0.002(0.000-0.000) 0.058(0.060-0.060) 1.667(0.000-3.330) M 0.002(0.000-0.000) 128.800(48.10-209.50)   30.327(29.390-31.260) Last 0.005(0.000-0.010) 0.001(0.000-0.000) 93.750(62.50-125.00) P value 0.160 0.078 0.106 Bacteria 0 h 0.043(0.020-0.070) 0.904(0.320-1.490) 0.043(0.020-0.070) 24 h 0.007(0.000-0.010) 0.046(0.010-0.080) 0.007(0.000-0.010) M 0.000(0.000-0.000) 12.798(0.540-25.050) 0.000(0.000-0.000) Last 0.013(0.000-0.070) 1.759(0.600-2.920) 0.000(0.000-0.000) P value 0.121 0.212 0.121 Colostrum & 0 h 0.600(0.330-0.870) 0.130(0.070-0.180) 0.012(0.010-0.020) Bacteria 24 h 0.001(0.000-0.000) 0.056(0.020-0.090)  222.78(145.50-300.06) M 0.002(0.000-0.000) 20.951(3.190-38.710) 85.565(53.92-117.21) Last 0.002(0.000-0.000) 0.009(0.000-0.010)  78.125(62.500-93.750) P value 0.104 0.104 0.112

In the model of MRSA infection, administration of camel colostrum raised TNF-α levels to 0.56 pg/ml, compared to 0.03 pg/ml for the administration of mixed colostrum. The greatest increase in TNF-α levels was observed for camel colostrum, which recorded 0.69 pg/ml. These results are summarized in Table 25 and FIG. 21 . The month-long experimental results are summarized in Table 26 and FIGS. 22A-22C.

TABLE 25 MRSA and TNF-α Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Type: Camel Bovine Mix P value^(A) Healthy 0.00(0.00-0.60) 0.00(0.00-0.60) 0.00(0.00-0.60) 1.000 Colostrum 0.56(0.00-0.94)  0.00(0.00-194.80) 0.03(0.00-0.62) 0.261 Bacteria 1.17(0.50-4.15) 0.00(0.00-0.00) 1.17(0.50-4.15) 0.002 Colostrum & Bacteria 0.69(0.00-4.73) 0.00(0.00-0.00)   0.08(0.00-3707.00) 0.013 P value^(b) 0.064 0.118 0.050 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(b)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

TABLE 26 MRSA and TNF-α Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.300(0.000-0.600) 0.300(0.000-0.600) 0.300(0.000-0.600) 24 h 0.220(0.000-0.440) 0.220(0.000-0.440) 0.220(0.000-0.440) M 0.269(0.000-0.540) 0.269(0.000-0.540) 0.269(0.000-0.540) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.000(0.000-0.000) P value 0.675 0.675 0.675 Colostrum 0 h 0.558(0.540-0.580) 0.000(0.000-0.000) 0.000(0.000-0.000) 24 h 0.828(0.720-0.940) 0.000(0.000-0.000) 0.000(0.000-0.000) M 0.430(0.170-0.690) 104.749(14.70-194.80)  0.177(0.050-0.300) Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.490(0.360-0.620) P value 0.108 0.077 0.078 Bacteria 0 h 2.884(1.620-4.150) 0.000(0.000-0.000) 2.884(1.620-4.150) 24 h 0.607(0.500-0.720) 0.000(0.000-0.000) 0.607(0.500-0.720) M 0.000(0.000-0.000) 0.000(0.000-0.000) 0.000(0.000-0.000) Last 1.166(0.500-4.150) 0.000(0.000-0.000) 0.000(0.000-0.000) P value 0.121 1.000 0.121 Colostrum & 0 h 4.098(3.470-4.730) 0.000(0.000-0.000) 0.000(0.000-0.000) Bacteria 24 h 1.422(0.940-1.910) 0.000(0.000-0.000) 0.000(0.000-0.000) M 0.383(0.330-0.440) 0.000(0.000-0.000) 1853.58(0.16-3707.00)  Last 0.000(0.000-0.000) 0.000(0.000-0.000) 0.622(0.560-0.680) P value 0.080 1.000 0.109

In the model of MRSA infection, administration of mixed colostrum raised IL-10 levels during the extended testing period to similar levels observed for S. aureus. Moreover, the administration of bovine colostrum increased IL-10 to 0.810 pg/ml after 24 hours. These results are summarized in Table 27 and FIG. 23 . The month-long experimental results are summarized in Table 28 and FIGS. 24A-24C.

TABLE 27 MRSA and IL-10 Immune Response in the Presence of Colostrum (Expressed as Median pg/ml (Min-Max)) Colostrum Type: Camel Bovine Mix P value^(A) Healthy  0.00(0.00-36.76)  0.00(0.00-36.76)  0.00(0.00-36.76) 1.000 Colostrum  0.00(0.00-16.30)  0.14(0.00-38.65)  83.30(0.00-1000.00) 0.115 Bacteria 0.00(0.00-0.00) 0.04(0.02-0.34) 0.00(0.00-0.00) 0.001 Colostrum & Bacteria 0.00(0.00-0.04) 0.03(0.00-6.41)  0.01(0.00-500.00) 0.035 P value^(B) 0.057 0.348 0.002 ^(A)= Comparison between different treatments within a single Colostrum type using a Nonparametric Test (Kruskal-Wallis Test). ^(B)= Comparison between different Colostrum types in each treatment using a Nonparametric Test (Kruskal-Wallis Test).

TABLE 28 MRSA and IL-10 Immune Response in the Presence of Colostrum at 0 h, 24 h, 7-25 days (M), and 30 days (Last) (Expressed as Median(Min-Max)) Treatment Time Camel Bovine Mix Healthy 0 h 0.016(0.000-0.030) 0.016(0.000-0.030) 0.016(0.000-0.030) 24 h 18.378(0.000-36.760) 18.378(0.000-36.760) 18.378(0.000-36.760) M 0.018(0.000-0.030) 0.018(0.000-0.030) 0.018(0.000-0.030) Last 0.004(0.000-0.010) 0.004(0.000-0.010) 0.004(0.000-0.010) P value 0.935 0.935 0.935 Colostrum 0 h 0.000(0.000-0.000) 19.621(0.590-38.650) 0.001(0.000-0.000) 24 h 0.000(0.000-0.000) 0.810(0.150-1.470) 0.002(0.000-0.000) M  8.152(0.000-16.300) 0.077(0.020-0.130)  166.63(166.60-166.66) Last 0.005(0.000-0.000) 0.001(0.000-0.000) 750.00(500.0-1000.0) P value 0.105 0.104 0.091 Bacteria 0 h 0.000(0.000-0.000) 0.207(0.070-0.340) 0.000(0.000-0.000) 24 h 0.000(0.000-0.000) 0.024(0.020-0.020) 0.000(0.000-0.000) M 0.000(0.000-0.000) 0.037(0.030-0.050) 0.000(0.000-0.000) Last 0.000(0.000-0.000) 0.036(0.030-0.040) 0.000(0.000-0.000) P value 1.000 0.108 1.000 Colostrum & 0 h 0.019(0.000-0.040) 1.089(0.030-2.150) 0.008(0.000-0.010) Bacteria 24 h 0.000(0.000-0.000) 3.225(0.040-6.410) 0.006(0.000-0.010) M 0.001(0.000-0.000) 0.034(0.020-0.040) 0.006(0.000-0.010) Last 0.003(0.000-0.000) 0.002(0.000-0.000)  500.00(500.00-500.00) P value 0.392 0.198 0.222

Overall, the S. aureus lethal dose experiments confirm that treatment with bovine colostrum resulted in lower stimulation of immune system cytokines than other tested treatments. For example, both the administration of colostrum mix alone and the administration of colostrum mix and the lethal dose of bacteria resulted in the same increase in IL-10 levels (83.30 pg/ml compared to administration of bacteria alone at 0.07 pg/ml) Administration of mixed colostrum alone and administration of mixed colostrum and bacteria raised IL-10 levels to 166.63 pg/ml at days 7-25 (M) and to 750.00 pg/ml by the final day of the experiment. Both camel colostrum and mixed camel colostrum and bovine colostrum stimulated TNF-α levels. The most enormous change was for camel colostrum in all treatments, which resulted in 0.56 pg/ml, 0.50 pg/ml, and 1.21 pg/ml for colostrum alone, bacteria alone, and colostrum and bacteria respectively.

Example 5 Calculating Correlations Between the Studied Cytokines and the Colostrum Sources

The immunomodulatory effect of pro-inflammatory cytokines varied depending upon the bacterial species tested. IFN-γ exhibited a steady level of immune response in mixed colostrum treatment (93.750 pg/ml in the E. coli model). In the S. aureus model, IFN-γ levels increased to 78.10 pg/ml when the mixture of colostrum was administered compared to 17.82 pg/ml in the control colostrum. In the MRSA experiments, IFN-γ levels increased to 78.13 pg/ml when the mixed colostrum was administered. TNF-α, in the P. aeruginosa experiments showed the most considerable change in level when camel colostrum and bacteria were administered (8.931 pg/ml after 24 hours compared to 1.171 pg/ml for bacterial injection only).

IL-10 is a crucial cytokine marker. In E. coli treated with mixed colostrum, IL-10 was elevated to 83.30 pg/ml compared to 31.62 pg/ml when bacteria alone were administered. Early cytokine transcriptional changes could be useful as a forecasting tool. IL-10 started to increase after 24 hours in the E. coli experiments, up to 80.3080 pg/ml. In S. aureus administered mixed colostrum and bacteria, IL-10 levels rose to 166.60 pg/ml after 7-25 days, and this increase was sustained over time and ended with 750.00 pg/ml after one month.

The best survival effect was in camel colostrum and mixed colostrum for all the tested bacteria (83% in E-coli-100% in MRSA) in the infected rats in the presence of colostrum.

Camel colostrum and mixed colostrum blocked adherence of bacteria to cultured tissue cells. Mixed colostrum (bovine colostrum and camel colostrum) can stimulate the immune response more than the bovine colostrum or camel colostrum alone. Colostrum has been shown to be a constant source of potentially probiotic bacteria in an infant's gut, including staphylococci, streptococci, and lactic acid bacteria. The immunomodulatory effect of pro-inflammatory cytokines varied due to the bacterial species.

IL-10 and IFN-γ showed a significant interaction at 24 hours. The significant elevations of the IL-10 and TNF-α transcriptional levels most likely indicate their essential role in the regulation of the immune responses of the bovine mammary gland in S. aureus infection. That could reflect the suppressive nature of the S. aureus mastitis. Early cytokine transcriptional changes could be useful as a forecasting tool in the detection of the subclinical S. aureus mastitis. The transcriptional patterns of these cytokines in the early stages of S. aureus infection could help to unravel their role in the pathophysiology of S. aureus mastitis. Finally, vital, crucial cytokine marker(s) could emerge that provide efficient diagnostic and therapeutic means for the early detection of S. aureus mastitis. Early cytokine transcriptional changes could be useful as a forecasting tool in the detection of the subclinical S. aureus mastitis.

These experiments demonstrate that camel colostrum, bovine colostrum and mixed colostrum (bovine and camel colostrum) can provide protective and immune-stimulatory effects against the studied pathogenic bacteria in vitro and in vivo. The lyophilized colostrum derivative studied maintained most of the bioactive factors that appear to be at the basis of its many nutritional, modulatory, or even therapeutic, applications.

The fastest and the best-protected treatment was for lethal S. aureus with a baseline of 50-100% mortality. 100% survival was obtained for all six rats injected with S. aureus and administered the three types of colostrum by i.p. injection. Camel colostrum had a tremendous protective effect from lethal MRSA, demonstrating 100% survival versus 100% mortality in MRSA administration alone. Also, MRSA showed the highest maximum increased values in % change in weight of rats administered mixed colostrum (43% compared to −21% for rats administered only the lethal dose of MRSA).

Camel colostrum and mixed colostrum alone induced a remarkable increase in the weight of rats ranging from (6%-59%). Bacterial injection led to a dramatic decrease in the percent weight change in rats from −12% to 12%. MRSA demonstrated the most significant maximum increased values in percent change of weight of rats treated with mixed colostrum (43% compared to −21% when administered MRSA alone).

Calculations of the correlation between IFN-γ, IL-10, and TNF-α are summarized in Tables 29-31. Table 29 shows that without the presence of Colostrum, the value of the correlation coefficient between IL-10 and TNF-α was −0.773**, indicating a significant negative strength of association, while the value of the correlation coefficient between IFN-γ and TNF-α was 0.464*, demonstrating a less significant positive strength of association. With the presence of Colostrum, the only significant value of the correlation coefficient was 0.647**, between IL-10 and IFN-γ. In the absence of Colostrum, the administration of bacterial strains did not demonstrate a significant value of the correlation coefficient between the three tested cytokines in gram negative E. coli and P. aeruginosa; however, gram-positive S. aureus and MRSA has significant values of the correlation coefficient between IL-10 and IFN-γ. In the presence of both Colostrum and bacterial strains, the correlation coefficient between IL-10 and IFN-γ demonstrated a positive strength of association for S. aureus (0.701*) and MRSA (0.503*). Further, in the presence of E. coli, the correlation coefficient between IL-10 and TNF-α had a significant negative strength of association (−0.470*).

Table 30 shows the correlation between IFN-γ, IL-10, and TNF-α in the presence of Colostrum when treated with S. aureus or MRSA. A significant value of a correlation coefficient was observed in the presence of Camel Colostrum, with the coefficient between IL-10 and TNF-α having a negative strength of association for S. aureus of −0.517** and for MRSA of −0.585**. A significant value of a correlation coefficient was observed in the presence of Bovine Colostrum, with the coefficient between IFN-γ and TNF-α having a positive strength of association for S. aureus of 0.415* and for MRSA of 0.551**. A number of significant values of correlation coefficients were observed in the presence of Mixed Camel and Bovine Colostrum, with the coefficient between IFN-γ and IL-10, IFN-γ and TNF-α, and IL-10 and TNF-α all having respective positive strength of association for S. aureus of 0.659**, 0.694**, and 0.439*. For MRSA, the coefficient between IFN-γ and IL-10 also showed a positive strength of association of 0.512**.

TABLE 29 Correlation between IFN-γ, IL-10, and TNF-α R (Spearman Treatments Parameters Correlation) Sig. Healthy IFN-γ with IL10 −0.036 0.867 N^(b) IFN-γ with TNF-α 0.464* 0.022 P^(a) IL10 with TNF-α −0.773** 0.000 N^(b) Colostrum IFN-γ with IL10 0.647** 0.001 P^(a) IFN-γ with TNF-α 0.269 0.203 P^(a) IL10 with TNF-α 0.025 0.908 P^(a) E. coli IFN-γ with IL10 0.242 0.267 P^(a) IFN-γ with TNF-α 0.056 0.811 P^(a) IL10 with TNF-α −0.295 0.207 N^(b) Colostrum & IFN-γ with IL10 0.353 0.151 P^(a) E. coli IFN-γ with TNF-α −0.144 0.557 N^(b) IL10 with TNF-α −0.470* 0.049 N^(b) P. aeruginosa IFN-γ with IL10 0.490 0.054 P^(a) IFN-γ with TNF-α −0.226 0.384 N^(b) IL10 with TNF-α −0.329 0.214 N^(b) Colostrum & IFN-γ with IL10 0.186 0.418 P^(a) P. aeruginosa IFN-γ with TNF-α −0.082 0.732 N^(b) IL10 with TNF-α 0.150 0.528 P^(a) S. aureus IFN-γ with IL10 0.755** 0.000 P^(a) IFN-γ with TNF-α −0.168 0.443 N^(b) IL10 with TNF-α −0.278 0.211 N^(b) Colostrum & IFN-γ with IL10 0.701** 0.000 P^(a) S. aureus IFN-γ with TNF-α 0.061 0.782 P^(a) IL10 with TNF-α −0.135 0.550 N^(b) MRSA IFN-γ with IL10 0.796** 0.000 P^(a) IFN-γ with TNF-α −0.512* 0.043 N^(b) IL10 with TNF-α −0.863** 0.000 N^(b) Colostrum & IFN-γ with IL10 0.503* 0.014 P^(a) MRSA IFN-γ with TNF-α 0.009 0.968 P^(a) IL10 with TNF-α −0.288 0.182 N^(b) *= Correlation is significant at the 0.05 level. **= Correlation is significant at the 0.01 level. ^(a)= Positive correlation. ^(b)= Negative correlation.

TABLE 30 Correlation between IFN-γ, IL-10, and TNF-α in the presence of colostrum for S. aureus and MRSA R (Spearman Colostrum Type Parameters Correlation) Sig. S. aureus Camel IFN-γ with IL10 0.140 0.452 P^(a) IFN-γ with TNF-α 0.090 0.628 P^(a) IL10 with TNF-α −0.517** 0.003 N^(b) Bovine IFN-γ with IL10 0.242 0.207 P^(a) IFN-γ with TNF-α 0.415* 0.020 P^(a) IL10 with TNF-α −0.290 0.121 N^(b) Mix IFN-γ with IL10 0.659** 0.000 P^(a) IFN-γ with TNF-α 0.694** 0.000 P^(a) IL10 with TNF-α 0.439* 0.013 P^(a) MRSA Camel IFN-y with IL10 0.116 0.566 P^(a) IFN-y with TNF-α 0.030 0.880 P^(a) IL10 with TNF-α −0.585** 0.001 N^(b) Bovine IFN-y with IL10 0.216 0.236 P^(a) IFN-y with TNF-α 0.551** 0.001 P^(a) IL10 with TNF-α −0.325 0.070 N^(b) Mix IFN-y with IL10 0.512** 0.005 P^(a) IFN-y with TNF-α 0.221 0.258 P^(a) IL10 with TNF-α −0.219 0.264 N^(b) *= Correlation is significant at the 0.05 level. **= Correlation is significant at the 0.01 level. ^(a)= Positive correlation. ^(b)= Negative correlation.

Table 31 shows the correlation between IFN-γ, IL-10, and TNF-α in the presence of Colostrum when treated with E. coli or P. aeruginosa. A significant value of a correlation coefficient was observed in the presence of Camel Colostrum, with the coefficient between IL-10 and TNF-α having a negative strength of association for E. coli of −0.595**. A significant value of a correlation coefficient was observed in the presence of Bovine Colostrum, with the coefficient between IFN-γ and TNF-α having a positive strength of association for E. coli of 0.559** and for P. aeruginosa of 0.548**. A number of significant values of correlation coefficients were observed in the presence of Mixed Camel and Bovine Colostrum, with the coefficient between IFN-γ and TNF-α having a positive strength of association for E. coli of 0.625** and for P. aeruginosa of 0.739**. Further, significant values of correlation coefficients were observed in the presence of Mixed Camel and Bovine Colostrum, with the coefficient between IFN-7 and IL-10 also showing a positive strength of association of 0.412* for E. coli and of 0.374* for P. aeruginosa.

TABLE 31 Correlation between IFN-γ, IL-10, and TNF-α in the presence of colostrum for E. coli and P. aeruginosa R (Spearman Colostrum Type Parameters Correlation) Sig. E. coli Camel IFN-γ with IL10 0.078 0.688 P^(a) IFN-γ with TNF-α −0.203 0.282 N^(b) IL10 with TNF-α −0.595** 0.001 N^(b) Bovine IFN-γ with IL10 0.345 0.057 P^(a) IFN-γ with TNF-α 0.559** 0.002 P^(a) IL10 with TNF-α −0.209 0.287 N^(b) Mix IFN-γ with IL10 0.413* 0.026 P^(a) IFN-γ with TNF-α 0.625** 0.000 P^(a) IL10 with TNF-α 0.210 0.274 P^(a) P. aeruginosa Camel IFN-γ with IL10 0.088 0.664 P^(a) IFN-γ with TNF-α −0.120 0.550 N^(b) IL10 with TNF-α −0.043 0.832 N^(b) Bovine IFN-γ with IL10 0.198 0.323 P^(a) IFN-γ with TNF-α 0.548** 0.003 P^(a) IL10 with TNF-α −0.277 0.162 N^(b) Mix IFN-γ with IL10 0.374* 0.038 P^(a) IFN-γ with TNF-α 0.739** 0.000 P^(a) IL10 with TNF-α 0.214 0.257 P^(a) *= Correlation is significant at the 0.05 level. **= Correlation is significant at the 0.01 level. ^(a)= Positive correlation. ^(b)= Negative correlation.

Overall, these examples illustrate at least that mixed colostrum can trigger a greater immune response than the administration of either bovine colostrum or camel colostrum alone. Further, the administration of any of the three colostrum groups increased survival against lethal doses of gram-positive and gram-negative bacteria, with camel colostrum and mixed colostrum providing the greatest increase in survival.

It is to be understood that the methods described herein are not limited to the specific embodiments described above, but encompasses any and all embodiments within the scope of the generic language of the following claims enabled by the embodiments described herein, or otherwise shown in the drawings or described above in terms sufficient to enable one of ordinary skill in the art to make and use the claimed subject matter. 

We claim:
 1. A colostrum composition comprising: a lyophilized colostrum and a saline solution, the lyophilized colostrum being made by the steps of: collecting colostrum from the mammary gland of a mammal; and freezing the colostrum at a temperature of at least −20° C. for at least a week; thawing the colostrum for at least 8 hours; and lyophilizing the colostrum; and wherein the lyophilized colostrum is suspended in the saline solution at a ration of 28 g lyophilized colostrum per liter saline solution to provide the colostrum composition.
 2. A natural pharmaceutical composition comprising the colostrum composition of claim 1 and a pharmaceutically acceptable carrier. 